Chronic musculoskeletal pain conditions are maladaptive and negatively impact the lives over 100 million Americans. A growing body of literature suggests that these chronic pain conditions result from imbalances in catecholamine homeostasis, which give way to increased release of pro-inflammatory molecules and increased activation of cells that transmit information about pain. Therefore, this proposal will employ a clinically-relevant animal model to [[1) determine if targeting specific pro-inflammatory molecules is able to reverse chronic pain caused by dysregulation of catecholamine homeostasis and 2) determine which cells involved in pain signal transmission play a role downstream from pro-inflammatory molecule activity.